Vascular endothelial cells can constrict and/or dilate blood vessels by releasing endothelium-derived nitric oxide (NO) and prostanoids and activating or degrading hormones related with vascular activity and thereby regulating the function of vascular smooth muscle.
As vascular endothelial cells age, their telomerase activity decreases. Also, aged vascular endothelial cells exhibit significantly decreased vasoconstiriction ability due to decreased NO production, endothelial nitric oxide synthase (eNOS) expression and prostacyclin production, facilitated thrombosis due to increased plasminogen activator type 1 (PAI-1) expression, and narrowing of blood vessels due to increased expression of cell adhesion molecules and chemokines such as intercellular adhesion molecule 1 (ICAM-1), interleukin-1 and interleukin-8 and increased inflammatory responses. Indeed, it is known that the vascular endothelial cells of arteriosclerotic tissues exhibit increased activity of senescence-associated beta-galactosidase (SA-β-gal), which is well known as a cellular aging marker, as compared to the cells of normal tissues. In addition, the cells of the arteriosclerotic tissues show shorter telomere length as compared to the cells of normal tissues.
Accordingly, it will be possible to prevent and treat cardiovascular diseases by preventing or postponing the aging of vascular endothelial cells. The best known method for delaying vascular aging is to restrict calorie intake. However, since this method is practically difficult to adopt and causes inconvenience in daily lives, an alternative method is necessary.